IL-10 Gene Promoter Polymorphisms in Rheumatoid Arthritis: SHORT REPORT

Hajeer, Ali H.; Lazarus, Mark; Turner, David M.; Mageed, Rizgar A.; Vencovský, Jiří; Sinnott, Paul J.; Hutchinson, Ian V.; Ollier, William

doi:10.1080/030097498441029

Cited by 130 publications

(17 citation statements)

References 8 publications

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“…Such an approach has been productive, and evidence has shown that corticotrophin releasing hormone [42], CYP19 (oestrogen synthase) [43], IFN-γ [44-46] and other cytokines [47-49] are linked to RA. Other approaches have addressed the possibility that genetic regions linked to other autoimmune diseases, such as insulin-dependent diabetes [50], may also be linked to RA.…”

Section: Genetic Factorsmentioning

confidence: 99%

Untitled

2002

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Chapter summaryThe prevalence of rheumatoid arthritis (RA) is relatively constant in many populations, at 0.5–1.0%. However, a high prevalence of RA has been reported in the Pima Indians (5.3%) and in the Chippewa Indians (6.8%). In contrast, low occurrences have been reported in populations from China and Japan. These data support a genetic role in disease risk. Studies have so far shown that the familial recurrence risk in RA is small compared with other autoimmune diseases. The main genetic risk factor of RA is the HLA DRB1 alleles, and this has consistently been shown in many populations throughout the world. The strongest susceptibility factor so far has been the HLA DRB1*0404 allele. Tumour necrosis factor alleles have also been linked with RA. However, it is estimated that these genes can explain only 50% of the genetic effect. A number of other non-MHC genes have thus been investigated and linked with RA (e.g. corticotrophin releasing hormone, oestrogen synthase, IFN-γ and other cytokines). Environmental factors have also been studied in relation to RA. Female sex hormones may play a protective role in RA; for example, the use of the oral contraceptive pill and pregnancy are both associated with a decreased risk. However, the postpartum period has been highlighted as a risk period for the development of RA. Furthermore, breastfeeding after a first pregnancy poses the greatest risk. Exposure to infection may act as a trigger for RA, and a number of agents have been implicated (e.g. Epstein–Barr virus, parvovirus and some bacteria such as Proteus and Mycoplasma). However, the epidemiological data so far are inconclusive. There has recently been renewed interest in the link between cigarette smoking and RA, and the data presented so far are consistent with and suggestive of an increased risk.

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Section: Genetic Factorsmentioning

confidence: 99%

Untitled

2002

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“…It controls the inflammatory procedures by suppressing the expression of proinflammatory cytokines, chemokines, adhesion molecules, and antigen-presenting and costimulatory molecules in monocytes/macrophages, neutrophils, and T cells [18, 26–28]. Several investigations of complex diseases have indicated a main role for IL-10 in chronic inflammatory disorders that are considered by the predominance of cytokines such as IL-1, IL-6, IL-8, IL-10, IL-12, and TNF.…”

Section: Discussionmentioning

confidence: 99%

“…Several investigations of complex diseases have indicated a main role for IL-10 in chronic inflammatory disorders that are considered by the predominance of cytokines such as IL-1, IL-6, IL-8, IL-10, IL-12, and TNF. These included Crohn's disease, psoriasis, multiple sclerosis, and rheumatoid arthritis [18, 26–28]. The exact mechanisms involved in the regulation of IL-10 production endure to be determined, although inherited factors seem to have imperative roles.…”

Section: Discussionmentioning

confidence: 99%

“…A difference in IL-10 secretion in association with a Single Nucleotide Polymorphism (SNP) in the -1082 position of the gene promoter has been established. In particular, an association of the -1082 G allele with a high IL-10 producing ability has been shown, through assessments of both mRNA and protein [18, 26–28]. The IL-10-1082 G/A SNP is located within an Ets binding site.…”

Section: Discussionmentioning

confidence: 99%

“…The IL-10-1082 G/A SNP is located within an Ets binding site. The -1082 A allele confers a higher binding empathy to the transcription factor PU.1, which inhibits gene expression and leads to decreased IL-10 expression in individuals carrying this allele [18, 26–28]; thus, it is reasonable that the IL-10-1082 GG and GA genotypes also have high expression rates in the premature lung.…”

Section: Discussionmentioning

confidence: 99%

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Association between Interleukin-10-1082 G/A and Tumor Necrosis Factor-α308 G/A Gene Polymorphisms and Respiratory Distress Syndrome in Iranian Preterm Infants

Khoshdel

Kheiri

Omidvari

et al. 2017

Mediators of Inflammation

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Cytokine polymorphisms may contribute to the prevalence of respiratory distress syndrome. The present study was done to investigate the frequency of interleukin- (IL-) 10 and tumor necrosis factor- (TNF-) α gene polymorphisms and their association with the risk of RDS in preterm infants. One-hundred and nineteen patients with RDS and 119 healthy preterm infants were enrolled. PCR restriction fragment length polymorphism was used to determine the frequency of IL-10 and TNF-α genotypes at -1082 A and -308 A, respectively. One-hundred and nineteen out of 238 infants had RDS (50%). The age of the mothers and gestational age ranged 17–45 (mean: 28.6 ± 5.3) years and 24–34 (mean: 34.3 ± 2.38) weeks, respectively. Totally, 23 deaths were recorded in the RDS group. Incidence of TNF-α-308 A/A and TNF-α-308 G/A was 84% and 16%, respectively. TNF-a-308 G/G was not found in both groups. Prevalence of IL-10-1082 G/G and IL-10-1082 G/A variants was 65.5% and 34.5%, respectively. IL-10-1082 A/A was not found in both groups. The incidence of the allele G in the IL-10-1082 polymorphism was lower in RDS group (P < 0.05). We found that the risk of RDS was correlated to sex, gestational age, and IL-10-1082.

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Evaluation of the response of primary human peripheral blood mononuclear phagocytes to challenge within vitro generated clinically relevant UHMWPE particles of known size and dose

Matthews

Besong

Green

et al. 2000

J. Biomed. Mater. Res.

200

143

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The response of primary human peripheral blood mononuclear phagocytes to challenge with clinically relevant ultra-high molecular weight polyethylene (UHMWPE) wear debris of known particle size and dose was evaluated. Particles with a mean size of 0.24, 0. 45, 1.7, 7.6, and 88 microm were cocultured with cells for 24 h before assessment of cell viability and production of the osteolytic cytokines interleukin (IL)-1 beta, IL-6, tumor necrosis factor-alpha, and granulocyte macrophage colony-stimulating factor, and prostaglandin E(2). All particle fractions were evaluated at particle volume (microm(3)) to cell number ratios of 10:1 and 100:1, which had been previously identified as being the most stimulatory and clinically relevant. None of the test fractions had an effect on cell viability. Whereas the heterogeneity of human individuals was clearly evident in the responses of the donors evaluated in this study (the response of donor 3 was between 5 and 20 times greater than the other donors), the most biologically active particles were found to be submicrometer in size. Stimulation with phagocytosable particles (0.24, 0.45, and 1.7 microm) resulted in enhanced levels of cytokine secretion. Macrophages stimulated with particles outside this size range produced considerably less cytokines at the volumes tested. These results confirm earlier findings and suggest that the size and volume of UHMWPE particles are critical factors in macrophage activation. Furthermore, they suggest that the heterogeneity of human individuals may be another important factor in determining implant life.

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IL-10 Gene Promoter Polymorphisms in Rheumatoid Arthritis: SHORT REPORT

Cited by 130 publications

References 8 publications

Untitled

Untitled

Association between Interleukin-10-1082 G/A and Tumor Necrosis Factor-α308 G/A Gene Polymorphisms and Respiratory Distress Syndrome in Iranian Preterm Infants

Evaluation of the response of primary human peripheral blood mononuclear phagocytes to challenge within vitro generated clinically relevant UHMWPE particles of known size and dose

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